Human respiration is governed by two systems of the brain, with one system located in the brain stem autonomously controlling involuntary contraction and relaxation of both the intercostal muscles and diaphragm, and the other in the cerebral cortex consciously controlling voluntary respiration. Oxygen level and pH balance over a functionally safe range in blood and tissue of human beings are autonomously maintained by lungs driven by the system in the brain stem whereas the system in the cerebral cortex can consciously alter the status of respiration without affecting vital function of the body dependent on the oxygenation and the pH balance. Kidneys also participate in maintaining the pH balance by reclaiming bicarbonate back to blood in case exhaling capacity of the lungs is exceeded to remove excess carbonic acid from blood. The conscious control of the respiration by the cerebral cortex not only affects frequency and depth of the contraction and relaxation of both the intercostal muscles and diaphragm but also utilizes voluntary muscles in pharynx, larynx and tongue. The voluntary muscles in the pharynx, larynx and tongue, together with associated involuntary muscles of these organs, form an inlet of airway for the lungs and help protect the lungs for autonomous gas exchange function.
Although disorders of the brain stem comprising medulla oblongata and pons are known to be responsible for well-recognized abnormalities of breathing such as Cheyene-Stokes respiration, these events are rare, occurring only in seriously ill patients who are likely hospitalized for terminal disorders. Consequently patients with the brain stem disorders require specially trained physicians and nurses who would need to rely on sophisticated equipments such as a ventilator to sustain life of the patients. On the other hand, there are a significantly larger number of people who have problems in the voluntary respiration while relatively functioning well for daily activities out in communities. These problems range from a simple snoring to significant obstructive sleep apnea, which occur during sleep but improve upon arousal and awakening. There are several well-identified causes for these problems, and it is presumed that one common denominator for these is an insufficient air intake across the inlet surrounded by the voluntary muscles of the pharynx, larynx and tongue. Loss of contractile muscle tone of the voluntary muscles and narrowing of the inlet by anatomical abnormalities have been attributed as most common causes of the problems and as such the mainstay of corrective measures for the problems has been to force air across the narrowed inlet into the lungs. This, the continuous positive airway pressure (CPAP) breathing, has been continuously improved in its methodology and equipment, yet it fundamentally requires a mask to fit to a mouth/nose of a patient while sleeping. Despite the limitation, the CPAP breathing has been accepted by the majority as the standard therapy of choice for the problems of voluntary breathing, based on its benign and effective noninvasive management and widespread acceptance by patients.
The loss of muscle tone of voluntary respiratory muscles is coincided with deepening stages of sleep that is known to reversibly reduce voluntary responses of an individual to external sensory stimuli. This process is believed to be mediated by blocking a portion of the thalamus that controls flow of external sensor stimuli to the cerebral cortex. Once the individual arouses or awakes, the cerebral cortex begins resuming activity that provides necessary muscle tone for the voluntary respiratory muscles, thereby maintaining a patient airway inlet. According to several studies, this thalamic-gating during sleep, however, is not complete but the brain is yet responsive to subconscious stimuli having a meaning to the individual or signaling danger from the environment (Coenen, 2010). For an example, sleeping subjects arose faster with spiking K complexes on EEG when hearing their own names than on hearing other names (Oswald, Taylor & Treisman, 1960). One study showed that sleeping subjects who were motivated to awake by presenting a specific stimulus awoke easier on these stimuli than non-motivated subjects (Zung & Wilson, 1961). Another study utilizing auditory stimuli and simultaneous recording of both EEG and fMRI in sleeping humans showed that parts of prefrontal cortex were more activated by stimuli having a specific significance than by neutral stimuli (Portas et al, 2000).
Auditory stimuli can be delivered through a cochlear (acoustic) branch of the vestibulo-cochlear nerve to the brain. The cochlear nerve receives auditory stimuli from a tympanic membrane in the ear canal and from bones surrounding the cochlear nerve structure. Efficiency of transmission of vibration in audible frequency is known to be better through bone conduction to the cochlear nerve than through air conduction via the tympanic membrane. This dual mode of transmission of vibration in audible frequency through the cochlear nerve allows fail-safe reception of external acoustic stimuli by the auditory complex of the brain.
Snoring comes from vibration of the airway inlet in the audible range of vibration, usually around 500 Hz in frequency, which is transmitted to soft tissue and bony structure of a skull of an individual. Snoring can be classified as primary snoring and secondary snoring. The primary snoring comes from palatal vibration at a frequency range of 20 Hz to 500 Hz whereas the secondary snoring is associated with sleep apnea occurring from non-palatal structure at a frequency of 500 Hz to 2000 Hz with a median around 1000 Hz (Pevernagie et al, 2008). People with the primary snoring continue to take in oxygen in a way they do not develop a significant drop in their oxygen saturation level in blood and tissue. In contrast, patients with an obstructive sleep apnea and the secondary snoring have a sequence of a short-lived initial snoring followed by a temporary blockade of the airway inlet by collapsing soft tissues and voluntary muscles of the throat to a point that there is no air movement across the blocked airway inlet multiple times during sleep. People with a moderate to severe sleep apnea are known to have ≥15 episodes of no breathing lasting 10 seconds or longer each night. Their brain generally does not wake them up in time before a significant drop in blood and tissue oxygen oftentimes to less than 90% of oxygen saturation (Crummy et al, 2007). In this instance, there won't be measurable vibrations from the airway inlet following the initial high pitch snoring until the patients become profoundly hypoxic.
Invasive-device-based management of a medical condition requires a careful risk-benefit evaluation, especially for its long-term implication of interactions with a human body. Over the past few years, there has been a great interest in direct electric stimulation of the nerves governing voluntary muscles of the airway inlet such as the hypoglossal nerve. Although it appears logical in an electromechanical engineering sense, there are significant flaws in this approach. Firstly, there has to be a solid establishment of a causal relationship between the snoring/obstructive sleep apnea and dysfunctioning cranial nerves, if there is any, including hypoglossal nerves. Additional gain of an increase in neuronal stimulation of the voluntary muscles of the airway inlet by the electrical stimulation may not be quantitatively significant when the cranial nerves are already functioning normal on their own, unless intensity of electrical neuronal stimulation exceeds a steady-state threshold of muscle contraction that on its own has no abnormal pathology to get corrected for. Secondly, we do not know a long-term outcome of electrically-stimulated cranial nerves, except that clinical study can only answer the long-term outcome regarding benefit, side effects and complications of the invasive placement of an electric device on or around cranial nerves. It is conceivable that there would be a range of risk involved in daily electric stimulation of cranial nerves since unlike electric cables, human nerve fibers are living cells which require constant renewal and maintenance at a molecular level. Damages to the nerves such as apoptotic death or atrophy of nerve cells, if occurred, may become permanent or semi-permanent for the majority of large trunk nerve fibers. It would take many years to study safety issues regarding functionality and viability of the electrically stimulated cranial nerves. Thirdly, it would be a hard sell for invasive placement of an electric stimulation device to people who have a mild to moderate obstructive sleep apnea that can be successfully managed by the CPAP breathing which is noninvasive.
There are devices which are to sense vibration of snoring/obstructive sleep apnea and to provide an individual with external stimuli including auditory stimuli to arouse the individual. Focusing only on measurable vibration of the airway inlet would miss occasions of cessation of breathing in case of complete apnea resulting in hypoxia of the individual since there would not be air movement across the airway inlet. For patients with a moderate to severe obstructive sleep apnea, the devices detecting vibration as a source of input data for generating external stimuli to the patients would not be able to help them avoid hypoxic conditions during episodes of apnea. In other instances, devices using air conduction to deliver external acoustic stimuli to the cochlear nerve requires an ear piece like an earphone an individual needs to wear during sleep. Issues of comfort with the earphone stuck in ear canals every night inevitably become an issue of compliance. Furthermore, the obstructive sleep apnea is more prevalent in older people who tend to develop decrease in hearing oftentimes due to conditions related to reduced air conduction of hearing such as disorders of the middle ear and ossification of the conduction apparatus in the middle ear.
To overcome these limitations, the present invention proposes that both the vibration of the airway inlet and decrease in tissue oxygen saturation be non-invasively detected as a source of input data for generating external acoustic stimuli to an individual, that the external acoustic stimuli be delivered through the bone conduction to the cochlear nerve, and that the external acoustic stimuli be relevant and specific to the individual to achieve high efficiency of the external acoustic stimulation to temporarily arouse the individual from a deep stage of sleep to a lighter stage of sleep at a time the airway inlet collapses due to relaxation of the voluntary muscles of the airway inlet. Preferably, initial set-up of the present invention would be done in a sleep laboratory that can monitor arousal responses and changes in snoring/apnea/hypoxia of an individual to various acoustic stimuli. Once a particular set of acoustic stimuli is chosen, it can be downloaded in a flash memory part of the present invention that works autonomously once activated.
Any repetitive stimuli to the brain are known to induce conditioned reflex that can wear off by increasing a threshold of response to the repetitive stimuli. This process may translate into a progressive loss of the arousal response to prolonged stimulation by the acoustic stimuli, thereby decreasing efficiency. In addition, direct exposure of the brain to adjacent electromagnetic radiation and radiofrequency waves emitting from any electrical devices is known to detrimental, although exact types of abnormal pathology related to a particular electromagnetic radiation or radiofrequency waves are not well established. The present invention proposes that arousal responses to stimuli be recorded for assessment of efficiency and that the brain of a user be shielded from radiofrequency waves generated by the present invention.